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PubMed1983

Five non-depolarizing muscle relaxants in precurarization.

Five different non-depolarizing muscle relaxants and a control solution of saline were studied as precurarization agents. Two hundred and twenty-two surgical patients (ASA I-II) were allocated in a double-blind fashion to one of the following groups: d-tubocurarine 0.05 mg/kg, alcuronium 0.03 mg/kg, pancuronium 0.01 mg/kg, gallamine 0.25 mg/kg, ORG NC-45 (vecuronium) 0.01 mg/kg and saline solution 0.005 ml/kg. Pretreatment was performed 4 min before administering a 1.5 mg/kg bolus of succinylcholine (SCh). Fasciculations, intubation conditions, duration of neuromuscular blockade after SCh, serum potassium changes and postoperative myalgias (in 60 patients) were recorded. All the drugs studied prevented fasciculations significantly (P less than 0.05) more than in the control group. d-Tubocurarine and alcuronium were superior to the others in this respect. Intubation conditions were best in the control and pancuronium groups, but there was no significant difference between the pancuronium and d-tubocurarine or between the d-tubocurarine and alcuronium groups. Pancuronium pretreatment prolonged the SCh block significantly, whereas other agents shortened the duration of the SCh block. The antagonism of the SCh block apparently also affected intubation conditions, although intubation remained satisfactory. A statistically significant rise in serum potassium level was measured only in the control and pancuronium groups. In the control and pancuronium groups, four patients out of 10 had postoperative myalgias, whereas in the other groups only one or none out of 10 had them (0/10 vs. 4/10; 0.10 greater than P greater than 0.05). In conclusion, d-tubocurarine and alcuronium seem to have advantages over pancuronium, ORG NC-45 and gallamine for precurarization.

Adolescent↗
PubMed2004

Effect of ephedrine on the onset time of succinylcholine.

BACKGROUND: The aim of this study was to evaluate the effect of ephedrine administered prior to induction of anaesthesia on the onset time of succinylcholine for endotracheal intubation. METHODS: Patients were randomly assigned to receive intravenously (i.v.) either 70 microg kg(-1) of ephedrine (Group I; n = 25) or saline (Group II; n = 25) 3 min before induction of anaesthesia. Induction of anaesthesia was provided with propofol 2 mg kg(-1) plus remifentanil 1 microg kg(-1). Onset time and duration of muscle fasciculation and onset time of succinylcholine were recorded. Intubation was attempted after establishment of 100% thumb relaxation and difficulties were recorded. Heart rate, pulse oxymetry (SpO2) and mean arterial pressure (MAP) were also recorded. RESULTS: The onset time of succinylcholine were significantly (P < 0.001) shorter in Group I (26 +/- 4 s), when compared with Group II (43 +/- 6 s). Patients in Group I were intubated at 49 +/- 7 s compared with 68 +/- 10 s in Group II. The score of intubation was similar in both groups. Duration of muscle fasciculation was longer in Group II. Heart rate and MAP increased significantly (P < 0.05) after ephedrine injection, compared with the baseline value in Group I. CONCLUSIONS: The onset time of succinylcholine can be shortened with ephedrine pretreatment.

Adolescent↗
PubMed1989

Accumulation of extracellular calcium at the endplate of mouse diaphragm after ecothiopate in vitro.

1. Experiments were carried out to investigate the accumulation from the extracellular medium of 45Ca2+ by the endplate region of skeletal muscle. 2. Mouse diaphragm muscle was incubated in physiological saline labelled with 45Ca at 37 degrees C for periods of up to 1.5 h. 3. The muscle was divided into junctional and non-junctional portions and the Ca from the extracellular fluid accumulated at the endplate determined from the 45Ca content of the portions. 4. The accumulation of extracellular Ca at the endplate region of muscles incubated in pysiological saline alone was nil, but there was accumulation in the presence of the anticholinesterase ecothiopate iodide 0.5 x 10(-6) M (ECO). Stimulation of the phrenic nerve at 0.02 Hz caused no further increase in accumulation but reduced the amount of spontaneous fasciculation. In tetrodotoxin (TTX) 10(-6) M, the accumulation was halved, and in 3.5 mM Mg2+ the accumulation was nil. Carbachol 10(-4) M resulted in an accumulation of Ca similar to that in ECO. 5. It is concluded that there was an accumulation of extracellular Ca following excitation of the nerve by stimulation at a low frequency and during the spontaneous fasciculations, and about half of the accumulation of extracellular Ca after ECO in the experiments was due to the postsynaptic action of ACh released non-quantally from the nerve terminals.

Animals↗
PubMed2003

Diazepam inhibits organophosphate-induced central respiratory depression.

OBJECTIVES: Current evidence suggests that mortality from acute organophosphate (OP) poisoning is partially mediated through central nervous system (CNS) respiratory center depression (CRD). However, the exact mechanism of OP-induced CRD is unknown. In these studies, the authors investigated the hypothesis that OP-induced CRD is the result of overstimulation of CNS respiratory centers. METHODS: Wistar rats received prophylaxis with either normal saline (controls), atropine, the peripherally acting anticholinergics glycopyrrolate (GLYC), ipratropium bromide (IB), or the CNS respiratory center attenuator diazepam. To determine if a dual CNS/peripheral cholinergic mechanism is responsible for animal death, two additional groups received combination treatment with diazepam plus either IB or GLYC. All treatments were completed 5 minutes before OP with subcutaneous dichlorvos. Differences in 10-minute and 24-hour mortality were assessed by the Fisher exact test. RESULTS: Dichlorvos poisoning resulted in profound fasciculations without obvious seizure in all cohorts. In controls and animals treated with peripherally acting anticholinergics, fasciculations were followed by sedation and respiratory arrest (0% 10-minute survival in all cohorts). In contrast, pretreatment with either atropine or diazepam significantly improved 10-minute survival (100% and 44%, respectively). Although GLYC or IB afforded no protection when given alone, when delivered in conjunction with diazepam, the combination significantly improved survival (both groups 88% at 24 hours), suggesting a dual CNS/pulmonary muscarinic mechanism of lethality. CONCLUSIONS: The central respiratory depressant diazepam paradoxically attenuates organophosphate-induced respiratory depression, and when combined with peripherally acting anticholinergic agents, reduces mortality in a rat model of severe acute OP poisoning.

Animals↗
PubMed2003

Early death due to severe organophosphate poisoning is a centrally mediated process.

OBJECTIVE: To distinguish whether early death from severe organophosphate (OP) poisoning with dichlorvos is mediated through peripheral or central nervous system (CNS) actions. METHODS: Wistar rats (n = 72) were randomized to pretreatment with either: normal saline (controls), peripheral anticholinergics (glycopyrrolate [low, medium, or high dose] or nebulized ipratropium bromide), or CNS + peripherally acting anticholinergics (diphenhydramine, nebulized atropine, or injected atropine). All treatments were given prior to a subcutaneous injection of 25 mg/kg dichlorvos (n = 8 per group). Survival was assessed at 10 minutes (early death) and 24 hours (delayed death). Kaplan-Meier (95% confidence intervals [95% CIs]) and chi-squared analysis was then performed to determine differences between treatments. RESULTS: Regardless of treatment, all animals exhibited profound nicotinic effects (fasciculations) without obvious seizures within 2 minutes of poisoning. In rats pretreated with peripherally acting agents, the fasciculations were rapidly followed by reduced motor activity, sedation, and death. Mortality at 10 minutes for saline controls, glycopyrrolate, and ipratropium was 88%, 96%, and 100%, respectively. The single control animal surviving beyond 10 minutes went on to develop peripheral cholinergic manifestations, including hypersalivation, urination, and defecation. Only one of 24 animals treated with injected atropine, nebulized atropine, or diphenhydramine died during the early phase of poisoning; all others survived to 24 hours (p < 0.01). CONCLUSIONS: Death in acute, severe OP poisoning is prevented by pretreatment with anticholinergic agents that cross the blood-brain barrier, but not by agents with only peripheral actions. Early death due to OP poisoning appears to be a centrally mediated process.

Animals↗
PubMed2005

Evaluation of chondroitin sulfate bioactivity in hippocampal neurones and the astrocyte cell line U373: influence of position of sulfate groups and charge density.

Chondroitin sulfates are linear polysaccharides of alternating glucuronic acid and N-acetylgalactosamine, sulfated in varying positions. They form the extracellular framework providing the information for the structural establishment of tissues in multicellular organisms. Growth cones of neurones modulate their outgrowth according to signals received from proteoglycans. The exact molecular structures behind these functions are not fully understood, but structural details of the carbohydrate backbone are crucial. In this report we have employed quantitative cytometry on hippocampal neurite outgrowth in the presence of chondroitin sulfate added in solution to determine the influence of the position and density of the sulfate groups of the N-acetyl-D-galactosamine-residues of chondroitin sulfates. It is of profound interest whether externally added chondroitin sulfates can compete with core protein bound chondroitin sulfate to modulate the effects of tissue-synthesized matrix. In series of microscopic images 3 parameters of neuritic outgrowth activity, neurite length, number of neurites and fasciculation (thickness of neurites) are analyzed at concentrations occurring in intact tissues. Fasciculation increased and number of neurites decreased with high di-sulfation. No significant differences on process length reduction were found between the isotypes. Specificity of effects found is emphasized, as no influence on cell proliferation with U373 human astrocyte cell line is detectable, while neurones clearly are inhibited. The IC30 and IC50 values of chondroitin sulfates isoforms are presented for neurones. The data indicate that the soluble fragments from chondroitin sulfate are actively modulating cell development. Besides dosage, sulfation density and position are relevant for effects of chondroitin sulfate in neuronal regenerative activity.

Animals↗
PubMed1988

Growth cone guidance in insects: fasciclin II is a member of the immunoglobulin superfamily.

The cellular cues that guide neuronal growth cones toward their targets are highly conserved in such diverse organisms as insects and vertebrates. Evidence presented here suggests that the molecular mechanisms underlying these events may be equally conserved. This article describes the structure and function of fasciclin II, a glycoprotein expressed on a subset of fasciculating axons in the grasshopper embryo. Antibody perturbation experiments suggest that fasciclin II functions in mediating one form of neuronal recognition: selective fasciculation. Fasciclin II is a member of the immunoglobulin gene superfamily and is homologous in structure and function to the neural cell adhesion molecule N-CAM and to several other vertebrate cell adhesion molecules.

Amino Acid Sequence↗
PubMed1984

Cell recognition during neuronal development.

Insect embryos, with their relatively simple nervous systems, provide a model system with which to study the cellular and molecular mechanisms underlying cell recognition during neuronal development. Such an approach can take advantage of the accessible cells of the grasshopper embryo and the accessible genes of Drosophila. The growth cones of identified neurons express selective affinities for specific axonal surfaces; such specificities give rise to the stereotyped patterns of selective fasciculation common to both species. These and other results suggest that early in development cell lineage and cell interactions lead to the differential expression of cell recognition molecules on the surfaces of small subsets of embryonic neurons whose axons selectively fasciculate with one another. Monoclonal antibodies reveal surface molecules in the Drosophila embryo whose expression correlates with this prediction. It should now be possible to isolate the genes encoding these potential cell recognition molecules and to test their function through the use of molecular genetic approaches in Drosophila.

Animals↗
PubMed1991

Diagnosis of motor neuron disease by neurologists: a study in three countries.

Ninety four neurologists in the United Kingdom, China, and West Germany responded to two structured questionnaires. The first assessed the diagnostic weighting assigned to a number of symptoms, signs, and clinical investigations ascertained from classical descriptions and case notes of patients with motor neuron disease (MND). The second tested the likelihood and consistency of diagnosis in a series of case summaries representing the clinical data of 10 patients with clinically and pathologically documented motor neuron disease. There was a wide measure of agreement concerning the common clinical features of the disease, especially regarding fasciculation of the tongue, fasciculation associated with weakness seen in more than one limb, and dysphagia. In the case summaries, however, there was clear variation in the ranked likelihood of the diagnosis of MND and in the consistency of diagnostic behaviour in the different groups of neurologists. These findings support the need for internationally agreed criteria in the diagnosis of MND. Any such criteria will need to be tested against a standardised data set to establish their validity.

China↗
PubMed1992

Biological monitoring of exposure to nerve agents.

Changes in acetylcholinesterase activity in blood and some organs of rats after intoxication with sarin, soman, VX, and 2-dimethylaminoethyl-(dimethylamido)-phosphonofluoridate (GV), in doses of roughly 2 x LD50 given intramuscularly, were obtained from published data and by experiment. The time course of inhibition of acetylcholinesterase in blood, regions of brain, and diaphragm and the occurrence of signs and symptoms of poisoning (none, salivation, disturbed ventilation and fasciculations, convulsions, or death) were summarised and compared. When blood enzyme activities were 70-100% normal, no obvious signs were seen; at 60-70%, salivation occurred; at less than 30-55%, disturbed ventilation and fasciculations were seen, and at 15-30%, convulsions occurred. Less than 10% was fatal. In experiments with narcotised dogs, the blood acetylcholinesterase activity and the ability to reactivate it with trimedoxime were determined after intoxication by intramuscular administration of the four compounds. It is concluded that acetylcholinesterase activity in the blood corresponds to that in the target organs and can be considered as an appropriate parameter for biological monitoring of exposure to nerve gases. Moreover, determination of reactivation of blood acetylcholinesterase gives more information than simple determination of enzyme activity.

Acetylcholinesterase↗
PubMed1977

Transient anterior horn cell dysfunction in diphenylhydantoin therapy.

A report on a patient who developed profuse fasciculations following diphenylhydantoin therapy for 30 months with subsequent complete recovery on cessation of therapy is presented. In view of the considerable variability of spontaneous potentials generated in spinal motor neurones, in vitro studies and pathological states with respect to shape, amplitude, frequency and duration, caution is advised in the assessment of the clinical significance of fasciculations. The possibility that our patient represents an instance of a 'reversible form of motor neuron disease' is entertained.

Adult↗
PubMed1997

Pralidoxime continuous infusion in the treatment of organophosphate poisoning.

OBJECTIVE: To report a case of organophosphate poisoning treated with a continuous infusion of pralidoxime chloride. CASE SUMMARY: A 27-year-old white man presented with extreme agitation, muscle weakness and fasciculations, and respiratory failure after ingesting an organophosphate pesticide (Dursban, active ingredients chlorpyrifos and xylene) as a suicide attempt. Atropine sulfate and pralidoxime chloride were administered intermittently, but the patient continued to be extremely agitated and have muscle fasciculations. Subsequently, a continuous intravenous infusion of pralidoxime (8 mg/mL concentration) at 500 mg/h was initiated to help control breakthrough nicotinic symptoms. Therapy with atropine and pralidoxime was continued for approximately 72 hours. Therapy was discontinued due to the predominance of anticholinergic symptoms and the patient's increased awareness. DISCUSSION: Severe organophosphate poisoning with nicotinic and/or central manifestations should be treated with pralidoxime in addition to atropine. The rationale supporting the use of pralidoxime as a continuous infusion in this case includes: (1) slow absorption of organophosphate compounds following exposure to large quantities, (2) unknown quantity ingested, (3) delayed nicotinic effects from redistribution of lipid-soluble organophosphate and metabolic activation of phosphorothioates such as chlorpyrifos, and (4) intensive care monitoring. There is limited documentation in the literature of continuous infusions of pralidoxime used to treat organophosphate poisoning and the stability of the admixture is unknown. CONCLUSIONS: A continuous pralidoxime infusion successfully managed the prolonged nicotinic symptoms seen after ingestion of an organophosphate. A continuous infusion of pralidoxime may be particularly useful in cases of organophosphate poisoning when the extent of chemical exposure or quantity of chemical ingested is unknown but potentially toxic and the therapy must be symptomatically managed.

Adult↗
PubMed2003

Clinical manifestations of VX poisoning following percutaneous exposure in the domestic white pig.

Nerve agents are a class of organophosphorus chemicals that inhibit certain cholinesterase enzymes (ChE). If untreated, percutaneous exposure to nerve agents, such as VX (O-ethyl-S-[2(diisopropylamino)ethyl] methylphosphonothioate) can cause paralysis, apnoea and death. Much of the information concerning the percutaneous absorption and subsequent toxicity of nerve agents has been obtained using various rodent models. However, the most relevant 'skin model' is arguably the pig. Therefore, the purpose of this study was to examine the clinical manifestations of VX intoxication in the domestic white pig following a 2 LD50 (120 microg/kg) percutaneous challenge. There was a consistent onset of signs (where present) in each animal: mastication was followed by miosis, salivation, fasciculations and apnoea. Whilst ChE activity did not correlate with the onset of signs, there was a qualitative relationship in that mastication preceded substantial ChE inhibition, miosis lagged behind the linear decrease in acetylcholinesterase (AChE) activity and fasciculations and apnoea occurred after maximum ChE inhibition had been attained (5-10% of normal). These observations may be of use for the triage of patients exposed to VX. In comparison with similar studies with GD, VX did not affect glucose utilization. However, VX was similar to GD in that it caused a mild hyperkalaemia and hyperphosphataemia, although the significance of this observation was not clear. There was substantial lateral diffusion of the initial droplet of VX over the application site, indicating that, when decontaminating exposed skin, attention should also be directed to areas peripheral to the original site of exposure.

Acetylcholinesterase↗
PubMed1991

Clinical and electrodiagnostic features of X-linked recessive bulbospinal neuronopathy.

We describe four men from two kinships affected with X-linked recessive bulbospinal neuronopathy, and one sporadic case. All developed postural tremor, weakness, and fasciculations, with onset from age 25 to 39 years. Weakness began in the pelvic girdle or hands, with dysphagia or dysarthria occurring years later in two. Sensory symptoms were present in only one, who also had diabetes mellitus. In contrast, sural nerve action potentials were small or absent in all. Needle EMG showed widespread chronic partial denervation with reinnervation. The characteristic twitching of the chin produced by pursing of the lips consisted of repetitive or grouped motor unit discharges, rather than fasciculations. Broader awareness of the distinctive features of bulbospinal neuronopathy will probably increase the frequency of its recognition. Diagnosis is important for purposes of providing a prognosis for affected men and genetic counseling for affected families.

Action Potentials↗
PubMed1999

Myasthenia, thymoma, presynaptic antibodies, and a continuum of neuromuscular hyperexcitability.

BACKGROUND: Autoantibodies specific for the nicotinic acetylcholine receptor (AChR) of skeletal muscle impair neuromuscular transmission in myasthenia gravis (MG). Autoantibodies specific for alpha3 neuronal AChRs or voltage-gated potassium channels have been reported in patients with Isaacs syndrome, an acquired disorder of continuous muscle fiber activity characterized by neuromyotonia. OBJECTIVE: To report the neuromuscular autoantibody profiles of three patients with a syndrome of MG and neuromuscular hyperexcitability. RESULTS: All three patients reported here had clinical and electrophysiologic evidence of MG and neuromuscular hyperexcitability. None had neuromyotonia. Thymoma was proven in two patients and suspected in the third. One had MG and thymoma and subsequently developed cramp-fasciculation syndrome; MG and rippling muscle syndrome appeared simultaneously in the other two. All patients had muscle and neuronal AChR binding antibodies and striational antibodies. Only one had antibodies reactive with alpha-dendrotoxin-complexed potassium channels. CONCLUSIONS: The coexistence of cramp-fasciculation syndrome and acquired rippling muscle syndrome with MG, thymoma, and neuronal AChR autoantibodies suggests that there is a continuum of autoimmune neuromuscular hyperexcitability disorders related pathogenically to Isaacs syndrome. Manifestations of neuromuscular hyperexcitability may be altered and less apparent in the context of MG because of the coexisting defect of neuromuscular transmission.

Adult↗
PubMed2002

The overlap of amyotrophic lateral sclerosis and frontotemporal dementia.

Patients with frontotemporal dementia (FTD) with no known diagnosis of ALS or family history of ALS were clinically and electrophysiologically assessed for the presence of ALS. Of 36 patients studied, five met criteria for a definite diagnosis of ALS and two had EMG findings suggestive of denervation in one limb. An additional five patients had prominent fasciculations and six other patients had trouble swallowing but all had normal results on EMG studies. One of the patients with fasciculations and a normal EMG study progressed to definite ALS over the course of 1 year.

Adult↗
PubMed1991

Pretreatment with d-tubocurarine, vecuronium, and pancuronium attenuates succinylcholine-induced increases in plasma norepinephrine concentrations in humans.

We studied in patients the effect of d-tubocurarine, which has sympathetic ganglion blocking action, on succinylcholine-induced increases in plasma levels of catecholamines, and compared it with the effects of vecuronium and pancuronium, which have little sympathetic ganglion blocking action. Thirty-two patients were divided into five groups: seven were given 3 mL saline; seven received 1 mg/kg succinylcholine; and six, seven, and five patients were given 0.08 mg/kg d-tubocurarine, 0.01 mg/kg vecuronium, and 0.01 mg/kg pancuronium, respectively, all of which were injected 5 min before 1 mg/kg succinylcholine. Succinylcholine alone significantly increased plasma norepinephrine concentrations, systolic blood pressure, and heart rate from 187 +/- 39 pg/mL (mean +/- SEM), 93 +/- 2 mm Hg, and 77 +/- 4 beats/min to 429 +/- 61 pg/mL, 120 +/- 7 mm Hg, and 102 +/- 6 beats/min, respectively, with onset of fasciculations. Pretreatment with d-tubocurarine, vecuronium, and pancuronium significantly and equally attenuated both the fasciculations and the cardiovascular responses to succinylcholine. These results suggest that the sympathetic ganglion blocking action of neuromuscular relaxants when given before succinylcholine is not an important factor in attenuation of succinylcholine-induced increases in plasma levels of catecholamines.

Adult↗
PubMed2005

A GFP-based genetic screen reveals mutations that disrupt the architecture of the zebrafish retinotectal projection.

The retinotectal projection is a premier model system for the investigation of molecular mechanisms that underlie axon pathfinding and map formation. Other important features, such as the laminar targeting of retinal axons, the control of axon fasciculation and the intrinsic organization of the tectal neuropil, have been less accessible to investigation. In order to visualize these processes in vivo, we generated a transgenic zebrafish line expressing membrane-targeted GFP under control of the brn3c promoter/enhancer. The GFP reporter labels a distinct subset of retinal ganglion cells (RGCs), which project mainly into one of the four retinorecipient layers of the tectum and into a small subset of the extratectal arborization fields. In this transgenic line, we carried out an ENU-mutagenesis screen by scoring live zebrafish larvae for anatomical phenotypes. Thirteen recessive mutations in 12 genes were discovered. In one mutant, ddl, the majority of RGCs fail to differentiate. Three of the mutations, vrt, late and tard, delay the orderly ingrowth of retinal axons into the tectum. Two alleles of drg disrupt the layer-specific targeting of retinal axons. Three genes, fuzz, beyo and brek, are required for confinement of the tectal neuropil. Fasciculation within the optic tract and adhesion within the tectal neuropil are regulated by vrt, coma, bluk, clew and blin. The mutated genes are predicted to encode molecules essential for building the intricate neural architecture of the visual system.

Animals↗